Purpose :
the purpose of this study was to investigate the relationships between dry eye disease (DED) and obesity and to outline the mechanism by which obesity may lead to the development of DED. In a population-based cohort, we attempted to identify the relationships between DED and obesity. Also, using the db/db mouse model of obesity, pathologic changes in functional units of tear production were investigated in relation to changes in molecular markers of obesity.

Methods :
Seven hundred twenty three cohort members, as well as male C57BL/KsJ-db/db mice for obesity (OB) and C57BL/KsJ-db/m mice for non-obese (NOB) controls were used for the present study. Patients were interviewed via a questionnaire to obtain information on socio-demographic characteristics and ocular surface disease index (OSDI) score, while blood sugar, and lipids were measured. For in vivo study, db/db and db/m male mice were used as a model of obesity and controls, respectively. A controlled environmental chamber was used to induce dry eye stress. Mice were scarified serially to obtain lacrimal glands (LGs) and corneas for measuring adipogenic factors and inflammatory cells with qPCR, ELISA, immunoblot, and flow cytometry.

Conclusions :
Irrelative with hyperlipidemia, obesity is an independent risk factor for DED and contributes to the development and progression of DED, as fat cells infiltrate LGs. NPY and its receptor Y1 plays an essential role for obesity-induced DED and LG changes and may be targets for treating and preventing the DED progression.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.